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缺氧引起红细胞增多,过去皆认为是缺氧对骨髓直接刺激的结果。但Rosin及Pachnilewitz(1948)曾用骨髓培养证明:缺氧非但不能促进,而且还要抑制骨髓的红细胞生成。说明缺氧在机体中之所以能促进红细胞生成,必然与某种中间体液调节有关。早在50多年前,Ca(?)not及Deflandre(1906)即曾发现,放血后贫血的兎血清中含有一种血液生成素(Hemopoietin,目前已改称红细胞刺激因子Erythrocyte stimulating factor,或促红细胞生成素Erythropoietin,以下简称EPT)的物质;1950年Reissman用联体动物再予证实后,近十余年来对这一因子的研究,已引起广大生理学、临床医学和航空医学工作者的注意,并已积累了大量实验与临床的资料。近年来,国内对这一因子的研究也在开展中。本文将最近几年来国外对EPT的实验研究成就作一简要介绍。
Hypoxia caused by increased red blood cells, the past are considered to be the result of direct stimulation of bone marrow hypoxia. But Rosin and Pachnilewitz (1948) have used bone marrow culture to prove: not only can not promote hypoxia, but also inhibit bone marrow erythropoiesis. Hypoxia in the body that can promote the formation of red blood cells, inevitably associated with some intermediate body fluid regulation. As early as more than 50 years ago, Ca (?) Not and Deflandre (1906) had found that blood after hemolysis anemia serum contains a hemoopoietin (Hemopoietin, has now been renamed erythrocyte stimulating factor Erythrocyte stimulating factor, or erythropoiesis Erythropoietin, hereinafter referred to as EPT) substances; Reissman re-affirmed with the syngeneic animal in 1950, nearly a decade of research on this factor has attracted the attention of the general physiology, clinical medicine and aviation medical workers, and Has accumulated a large number of experimental and clinical data. In recent years, the domestic research on this factor is also under way. This article will make a brief introduction of the achievements of EPT experiment abroad in recent years.